Dieldrin resistance in the malaria vector Anopheles gambiae in Ghana

• Published in: Medical and veterinary entomology Vol. 20; no. 3; pp. 294 - 299
• Main Authors: Brooke, B.D, Hunt, R.H, Matambo, T.S, Koekemoer, L.L, Van Wyk, P, Coetzee, M
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.09.2006
• Subjects: amino acid substitution; Animals; Anopheles - drug effects; Anopheles gambiae; biochemical; chromosome inversions; Culicidae; detoxifying enzymes; dieldrin; Dieldrin - pharmacology; dieldrin resistance; Diptera; enzyme activity; Female; GABA mutation; GABA receptors; gamma-aminobutyric acid; genetic resistance; Ghana; insect vectors; Insecticide Resistance; Insecticides - pharmacology; inversion polymorphism; pesticide synergists; Pesticide Synergists - pharmacology; piperonyl butoxide; Piperonyl Butoxide - pharmacology; resistance mechanisms; synergists; Ghana
• ISSN: 0269-283X; 1365-2915
• DOI: 10.1111/j.1365-2915.2006.00639.x

Anopheles gambiae Giles s.s. (Diptera: Culicidae) is one of the principal vectors of malaria in the Ashanti region of central Ghana. High levels of resistance to dieldrin were recorded in a wild-caught sample from Obuasi (south of Kumasi) as well as a laboratory colony established using material from the wild population. Cytogenetic analysis of wild-caught and laboratory samples revealed chromosomal polymorphism for inversions 2La and 2Rb. Although inversion 2La has previously been shown to be associated with dieldrin resistance in certain other laboratory strains originating from West Africa, there was no obvious association between inversion karyotype assortment and the resistance phenotype in the Obuasi population. In addition, polymerase chain reaction analysis indicated the presence of the alanine296 to glycine mutation in the GABA (γ? amino-butyric acid) receptor (which has been mapped to a chromosomal position within inversion 2La). This mutation has previously been shown to be associated with dieldrin resistance in the same An. gambiae laboratory strains of West African origin. Our data show only a weak association between the dieldrin resistance phenotype and the presence of this mutation, suggesting that another dieldrin resistance mechanism is operational in the Obuasi population. Biochemical and synergist exposure assays suggest a metabolic component, probably mediated by monooxygenase P450 enzymes. We conclude that dieldrin resistance in the An. gambiae population of the Obuasi region occurs at a high level - most likely in the absence of selection - and that control of the resistance phenotype is polyfactorial and must include components other than mutations in the GABA receptor locus.